Stimulation method for the sphenopalatine ganglia, sphenopalatine nerve, or vidian nerve for treatment of medical conditions

ABSTRACT

A method is provided for suppressing or preventing pain in a patient. One step of the method includes positioning first and second electrodes, without penetrating the cranium, on or proximate to at least one of the sphenopalatine ganglia, the sphenopalatine nerves, or the vidian nerves on both sides of the patient&#39;s face. At least one of a medication solution, an analgesic, or an electrical signal is then applied to at least one of the sphenopalatine ganglia, the sphenopalatine nerves, or the vidian nerves through the first and second electrodes. Pain signal generation in, or transmission through, the at least one of the sphenopalatine ganglia, sphenopalatine nerves, or vidian nerves is disrupted on both sides of the patient&#39;s face.

CROSS REFERENCES TO RELATED APPLICATIONS

The following application is a continuation of U.S. patent applicationSer. No. 12/372,124, filed Feb. 17, 2009, now U.S. Pat. No. 8,206,369which is a divisional application of U.S. patent application Ser. No.10/245,896, filed Sep. 17, 2002 (Now Abandoned), which is a divisionalapplication of application Ser. No. 09/595,784 filed Jun. 16, 2000 nowU.S. Pat. No. 6,526,318, issued Feb. 25, 2003. The followingcontinuation application claims priority to the aforementionedapplications for all purposes and incorporates the aforementionedapplications by reference in their entireties for all purposes.

FIELD OF THE INVENTION

The present invention relates generally to methods for suppressing orpreventing medical conditions such as pain, movement disorders, sleepdisorders, autonomic disorders, gastrointestinal disorders, and abnormalmetabolic states arising from signals generated by or transmittedthrough the sphenopalatine ganglia, the sphenopalatine nerve, or vidiannerve.

BACKGROUND OF THE INVENTION

Headaches are one of the most common ailments, and afflict millions ofindividuals. The specific etiology of headaches may be difficult topinpoint. Known sources of headache pain include trauma and vascular,autoimmune, degenerative, infectious, drug and medication-induced,inflammatory (sarcoid), neoplastic (primary or metastatic),metabolic-endocrine, iatrogenic (such as post-surgical), muscloskelataland myofascial causes. Even if the condition underlying the headachepain is identified and treated, headache pain may persist.

Diagnosis of headache pain will typically include an identification ofone or more categories of headaches. There are a variety of differentheadaches with different features. Migraine headaches, as defined by theInternational Headache Society (IHS) Classification, are typicallyunilateral, throbbing headaches lasting from four to seventy-two hours.Migraines are often accompanied by nausea, vomiting, light sensitivityand/or noise sensitivity. Females suffer from migraines more than malesby an approximate ratio of 3:1. Migraine headaches can be furthersubdivided and sub-classified into a number of different categories,such as, for example, migraine with aura, migraine without aura, andretinal migraine.

Migraines have traditionally been treated with medications to preventtheir recurrence and to alleviate acute pain and associated symptoms,such as nausea and vomiting. Non-invasive modalities of migrainetreatment, which may be used alone or in combination, have included:diet modification, which may include the avoidance of known headachetriggers (such as certain foods); biofeedback and relaxation techniquesas well as other psychological modalities; acupuncture; chiropracticmanipulation; and physical therapy. Invasive therapeutic procedures havealso been implemented, and have included localized anesthetic blocks aswell as neurosurgical interventions, such as nerve and gangliontransections and/or resections. Unfortunately, the effectiveness of eachtherapeutic modality typically varies widely between individual migrainesufferers, and irrespective of the treatment modality used, thesuppression of migraine pain is often short-lived, with the painrecurring at levels which are typically less but sometimes equally orrarely more intense than before treatment.

Newer techniques for treating a variety of neurological disorders haveincluded electrical stimulation of cranial nerves of the central nervoussystem, such as the glossopharyngeal, vagus, or trigeminal nerves. Forexample, U.S. Pat. No. 5,540,734 to Zabara describes a suggestedtherapeutic modality for a variety of medical, psychiatric andneurological disorders, including migraines, in which modulatingelectrical signals are applied to either or both of the trigeminal andglossopharyngeal nerves using electrodes. The principle behind theseapproaches is to disrupt or modulate abnormal neuronal transmissions inthe nervous system through the application of the modulating electricalsignals.

Cluster headaches are so termed due to their repeated occurrence ingroups or clusters. Cluster headaches are much less common thanmigraines: migraine sufferers outnumber cluster headache sufferers by aratio of approximately 100:1. Cluster headaches are characterized byintense, stabbing pain usually starting in the region of an eye ortemple and localizing to one side of the face. Autonomic features suchas lacrimation, nasal congestion, ptosis, conjunctival injection andpupillary changes are common in cluster headaches, which occurpredominantly (approximately 90%) in males and usually start in thethird or fourth decade of life. It is believed that the ingestion ofalcohol may trigger the onset of cluster headaches.

IHS criteria indicate that episodic attacks of cluster headaches maylast up to 90 minutes and may occur as many as six times per day.Cluster headaches typically occur in cycles lasting weeks to months andthen spontaneously remit. Frequently, cluster headaches have a seasonalcorrelation, with their onset occurring more often in the fall andspring. While there are wide variations in the start of cluster headachecycles between headache sufferers, the cycles experienced by individualheadache sufferers frequently follow a defined pattern with littledeviation. The headaches usually occur night, and often awaken theheadache sufferer from sleep. It is not unusual for individual headachesufferers to experience the onset of cluster headaches at the same timeduring the night over repeated nights.

Because of the typically short duration of cluster headaches, therapiesdesigned to abort the pain of an acute attack must have a quick onset ofaction. Such therapies have included oxygen inhalation, and injectionsof medication, such as dihydro ergotamine (DHE), ketorolac, orsumatripetan. Non-invasive therapies used to treat cluster headache painand prevent their recurrence have included use of medications includingergot derivatives, varapamil, lithium, steroids, and sodium valproate;psychological intervention with biofeedback and relaxation techniques;and acupuncture. Anesthetic agents (such as Lidocaine) have been appliedto the sphenopalatine ganglia, either directly, using a syringe, orindirectly, by soaking a long cotton swab in the anesthetic and placingthe swab intranasally adjacent to the sphenopalatine ganglia, such thatthe anesthetic diffuses through the nasal mucosa to affect the SPG.Invasive approaches for the treatment of cluster headaches have includedlocalized anesthetic block, surgical resection, radiofrequency,alcohol/phenol infiltration, radiosurgery and cryotherapy of thesphenopalatine ganglia and the trigeminal nerve and ganglion. Theinvasive approaches for treating cluster headaches are typically usedonly in headache sufferers who cannot tolerate the non-invasive methodsof treatment, or in whom the cluster headaches are refractory andinadequately controlled with non-invasive methods.

Neuralgias, such as trigeminal, sphenopalatine, and occipitalneuralgias, may start at any age, although trigeminal neuralgia is morecommon among the elderly. From a pathophysiological standpoint, painarising due to neuralgias always originates from and is transmitted bythe involved nerve. Accordingly, neuralgias may be caused by directinjury to nerves in the form of trauma, infection (such as herpes),neuroma formation or demyelination. Pain arising due to neuralgia may bebrief and paroxysmal or continuous, and numerous attacks may occurthroughout the day. Neuralgias do not feature seasonal or diurnalpatterns in the onset of pain. In contrast to cluster headaches,trigeminal neuralgia often has an associated “trigger zone” on the facewhich can trigger the onset of the pain. Sphenopalatine neuralgia oftenhas autonomic features, which are not commonly found in otherneuralgias. In occipital neuralgia, the occipital nerve is usuallytender to palpation and pain can be manifested anywhere along the courseof the nerve.

Neuralgias, like migraines, have been treated using medication, invasiveprocedures, and, rarely, electrical stimulation of cranial nerves whichare part of the central nervous system. None of the medications used intreating neuralgias have generally been effective in treating clusterheadaches, other than sodium valproate.

The use of medications to treat the above-described conditions canresult in systemic side-effects of wide-ranging severity. Invasivetechniques used to destroy tissues, such as lesioning, resecting,freezing, or burning, are typically non-reversible, and the treatmentcannot be adjusted once applied. Destruction of the tissue may itselflead to significant side effects, such as deafferentation pain.

A primary object of the present invention is to provide a method forpreventing or substantially suppressing pain and other medicalconditions without requiring the use of medications or destruction ofnerves or other tissues in the body.

A further object of the present invention is to provide a method forpreventing or substantially suppressing pain and other medicalconditions which can be utilized multiple times without successiveinvasive procedures.

Another object of the present invention is to provide a method forpreventing or substantially suppressing pain and other medicalconditions which can be adjusted to the patient's individual needswithout requiring further surgical intervention.

A yet further object of the present invention is to provide a method forpreventing or substantially suppressing pain and other medicalconditions which can be triggered and adjusted by the patient oversuccessive uses.

Other objects and advantages of the current invention will becomeapparent when the inventive stimulation method is considered inconjunction with the accompanying drawings, specification and claims.

SUMMARY OF THE INVENTION

A method is provided for the suppression or prevention of pain, movementdisorders, epilepsy, cerebrovascular diseases, autoimmune diseases,sleep disorders, autonomic disorders, urinary bladder disorders,abnormal metabolic states, disorders of the muscular system, andneuropsychiatric disorders in a patient. The method comprisespositioning at least one electrode on or proximate to at least one ofthe patient's sphenopalatine ganglia, sphenopalatine nerves, or vidiannerves, and activating the at least one electrode to apply an electricalsignal to at least one of those ganglia or nerves.

In a further embodiment of the invention used to treat the sameconditions, the electrode used is capable of being activated to dispensea medication solution or analgesic to at least one of the sphenopalatineganglia, sphenopalatine nerves, or vidian nerves.

A method is also provided for surgically implanting an electrode on orproximate to at least one of the sphenopalatine ganglia, sphenopalatinenerves, or vidian nerves of a patient. The surgical method comprisesmaking a first incision over the anterior portion of a coronoid notch ofthe patient and inserting an electrode introducer needle containing astylet into the first incision. The electrode introducer needle is thenadvanced in the direction of a point one-third of the vertical distancebetween the flares and the nasion of the patient until the needle isabout to encounter the lateral pterygoid plate of the patient. Theelectrode introducer needle is then advanced anteriorly until theelectrode introducer needle enters the pterygopalatine fossa. Theelectrode introducer needle is advanced further into the pterygopalatinefossa on a trajectory bringing the electrode introducer needle as closeas possible to the Vidian canal. The stylet is then removed from theelectrode introducer needle, and the electrode is placed in a centralchannel of the electrode introducer needle. The electrode is thenadvanced to a distal tip of the electrode introducer needle such thatthe electrode is placed on or proximate to at least one of thesphenopalatine ganglia, sphenopalatine nerves, or vidian nerves of apatient; at which point the electrode introducer needle is withdrawnwithout displacing the electrode from its position.

BRIEF DESCRIPTION OF TEE DRAWINGS

FIG. 1 is a schematic drawing of a lateral view of the skull showing theposition of the infratemporal fossa with the sphenopalatine ganglionlying within the sphenopalatine fossa, surrounded by the anterior marginof the lateral pterygoid plate and the posterior wall of the maxillarysinus.

FIG. 2 is a schematic diagram of a lateral view of the lateral nasalwall showing the position of the sphenopalatine ganglion directlyunderneath the nasal mucosa and located at the posterior margin of thesuperior and middle nasal turbinates.

DESCRIPTION OF THE PREFERRED EMBODIMENT

A first preferred embodiment of the inventive method utilizes direct andlocalized electrical stimulation of the sphenopalatine ganglion (“SPG”;also called the pterygopalatine ganglion), the sphenopalatine nerve(“SPN”; also called the pterygopalatine nerve) and/or the nerve of thepterygoid canal, also termed the vidian nerve (“VN”), using one or moresurgically implanted electrodes, for treatment of a number of medicalconditions. Medical conditions which may be treated by the inventivemethod include, but are not limited to: pain, movement disorders,epilepsy, cerebrovascular diseases, autoimmune diseases, sleepdisorders, autonomic disorders, urinary bladder disorders, abnormalmetabolic states, disorders of the muscular system, and neuropsychiatricdisorders.

Pain treatable by the inventive method may be caused by conditionsincluding, but not limited to: migraine headaches, including migraineheadaches with aura, migraine headaches without aura, menstrualmigraines, migraine variants, atypical migraines, complicated migraines,hemiplegic migraines, transformed migraines, and chronic dailymigraines; episodic tension headaches; chronic tension headaches;analgesic rebound headaches; episodic cluster headaches; chronic clusterheadaches; cluster variants; chronic paroxysmal hemicrania; hemicraniacontinua; post-traumatic headache; post-traumatic neck pain;post-herpetic neuralgia involving the head or face; pain from spinefracture secondary to osteoporosis; arthritis pain in the spine,headache related to cerebrovascular disease and stroke; headache due tovascular disorder; reflex sympathetic dystrophy, cervicalgia (which maybe due to various causes, including, but not limited to, muscular,discogenic, or degenerative, including arthritic, posturally related, ormetastatic); glossodynia, carotidynia; cricoidynia; otalgia due tomiddle ear lesion; gastric pain; sciatica; maxillary neuralgia;laryngeal pain, myalgia of neck muscles; trigeminal neuralgia (sometimesalso termed tic douloureux); post-lumbar puncture headache; lowcerebro-spinal fluid pressure headache; temporomandibular jointdisorder; atypical facial pain; ciliary neuralgia; paratrigeminalneuralgia (sometimes also termed Raeder's syndrome); petrosal neuralgia;Eagle's syndrome; idiopathic intracranial hypertension; orofacial pain;myofascial pain syndrome involving the head, neck, and shoulder; chronicmigraneous neuralgia, cervical headache; paratrigeminal paralysis;sphenopalatine ganglion neuralgia (sometimes also termed lower-halfheadache, lower facial neuralgia syndrome, Sluder's neuralgia, andSluder's syndrome); carotidynia; Vidian neuralgia; and causalgia; or acombination of the above.

Movement disorders treatable by the inventive method may be caused byconditions including, but not limited to: Parkinson's disease;cerebropalsy; dystonia; essential tremor; and hemifacial spasms.Epilepsy treatable by the inventive method may be, for example,generalized or partial. Cerebrovascular disease treatable by theinventive method may be caused by conditions including, but not limitedto: aneurysms, strokes, and cerebral hemorrhage. Autoimmune diseasestreatable by the inventive method include, but are not limited to,multiple sclerosis. Sleep disorders treatable by the inventive methodmay be caused by conditions including, but not limited to: sleep apneaand parasomnias. Autonomic disorders treatable by the inventive methodmay be caused by conditions including, but not limited to:gastrointestinal disorders, including but not limited togastrointestinal motility disorders, nausea, vomiting, diarrhea, chronichiccups, gastroesphageal reflux disease, and hypersecretion of gastricacid; autonomic insufficiency; excessive epiphoresis; excessiverhinorrhea; and cardiovascular disorders including but not limited tocardiac dysrythmias and arrythmias, hypertension, and carotid sinusdisease. Urinary bladder disorders treatable by the inventive method maybe caused by conditions including, but not limited to: spastic orflaccid bladder. Abnormal metabolic states treatable by the inventivemethod may be caused by conditions including, but not limited to:hyperthyroidism or hypothyroidism. Disorders of the muscular systemtreatable by the inventive method include, but are not limited to,muscular dystrophy and spasms of the upper respiratory tract and face.Neuropsychiatric disorders treatable by the inventive method may becaused by conditions including, but not limited to: depression,schizophrenia, bipolar disorder, and obsessive-compulsive disorder.

The inventive method acts to suppress or prevent these conditions bydisrupting sensory signals passing through the autonomic nervous system,including pain signals, as the signals traverse or are generated in theSPG, the SPN, or VN. The abnormal regulation of pain pathways, which maybe a feature of the conditions described as examples above, can causeexcitation or a loss of inhibition of those pathways, resulting in anincreased perception of pain. Direct electrical stimulation of the SPG,SPN, and/or VN can block the transmission of pain signals and stimulateinhibitory feedback of the pain pathways passing through the SPG, SPN,and/or VN, reducing or eliminating the pain experienced by the patient.Similarly, stimulation of the SPG, SPN, and/or VN can block thetransmission of signals other than pain which can provoke or aggravateother undesirable sensations or conditions, such as nausea, bladderdisorders, sleep disorders or abnormal metabolic states.

The autonomic system, which innervates pain pathways within the humanbody, consists of two divisions: the sympathetic and the parasympatheticsystems. The sympathetic and parasympathetic systems are antagonistic intheir action, balancing the other system's effects within the body. Thesympathetic system usually initiates activity within the body, preparingthe body for action, while the parasympathetic system primarilycounteracts the effects of the sympathetic system.

SPG, SPN, and VN structures are located on both sides of a patient'shead. The inventive method may be applied to apply stimulus to the SPG,SPN, and/or VN on either or both sides of the patient's head. Withreference to FIGS. 1 and 2, it shall be assumed for the followingdiscussion that the inventive method is being applied to the patient'sleft side.

Referring to FIG. 2, the SPG 102 is located behind the maxilla 103 inthe pterygopalatine fossa 126 posterior to the middle nasal turbinate138. The SPG 102 is surrounded by a layer of mucosal and connectivetissue of less than five millimeters in thickness. The SPG is part ofthe parasympathetic division of the autonomic nervous system. However,the SPG has both sympathetic and parasympathetic nerve fibers, as wellas sensory and visceral nerve fibers. The parasympathetic activity ofthe SPG is mediated through the greater petrosal nerve, while thesympathetic activity of the SPG is mediated through the deep petrosalnerve, which is essentially an extension of the cervical sympatheticchain. Sensations generated by or transmitted through the SPG include,but are not limited to, sensations to the upper teeth, feelings offoreign bodies in the throat, and persistent itching of the ear. Facialnerve and carotid plexuses directly communicate sensory signals to theSPG, and cell bodies in the ventral horn of the thoracolumbar spinalcord send fibers either directly or via cervical ganglion to the SPG.The SPG transmits sensory information, including pain, to the trigeminalsystem via the maxillary branch.

The deep and greater petrosal nerves 134 join together just beforeentering the pterygoid canal to form the VN 132. The VN 132 is housedwithin the Vidian canal 130, which is directly posterior to the SPG 102.The VN 132 connects to the SPG 102 and contains parasympathetic fiberswhich synapse in the SPG 102, sensory fibers which provide sensation topart of the nasal septum, and also sympathetic fibers.

The SPN 105 are sensory nerves that connect the SPG 102 to the maxillarynerve. The SPN 105 traverse through the SPG 102 without synapsing andproceed to provide sensation to the palate. The SPN 105 suspend the SPG102 in the pterygopalatine fossa.

Stimulation of the VN 132 and SPN 105 similarly may be used to suppressor prevent undesirable medical conditions by disrupting signals passingthrough the VN 132, most of which also pass through the SPG 102 due tothe interconnections between the VN 132 and SPG 102.

In the preferred embodiment of the invention, one or more electrodes aresurgically implanted directly on or adjacent to the SPG 102, SPN 105,and/or on the VN 132 of a patient. For purposes of clarity, in thefollowing discussion it shall be assumed that a single electrode isimplanted within the patient. However, it should be understood thatmultiple electrodes may be implanted according to the inventive method,and that the characteristics discussed with respect to the singleelectrode apply equally to additional electrodes utilized.

The electrode is preferably controllable to produce output stimulatingsignals which can be varied in voltage, frequency, pulse width, current,and intensity. Further, the electrode is also preferably controllablesuch that the controller may produce both positive and negative currentflow from the electrode, stop current flow from the electrode, or changethe direction of current flow from the electrode. The electrodepreferably also has the capacity for variable output, linear output, andshort pulse width. The electrode should be anchored securely at the siteof implantation within the patient so that the output signals producedby the electrode will consistently stimulate the same regions of theSPG, SPN, and/or VN. Electrodes suitable for this purpose are producedby Medtronics Corporation under the trade name Pisces Compact.

It is recommended that the application of stimulus from the electrodeand adjustments of the electrode parameters as described above will bedone under the supervision and guidance of a physician. However, itshould be understood that the inventive method may be applied such thatthe patient could, on the patient's initiative, activate the electrodeto stimulate the SPG, SPN, or VN. While it may be possible to configurethe electrode and its controller such that the patient could alter theparameters of the electrode stimulus without supervision by a physician,this would not be recommended as the patient may not have sufficientknowledge to avoid dangers associated with misapplication of theInventive method.

The electrode will be connected to a power source (such as a battery orpulse generator) which provides the energy source for the electricalstimulation. The power source may be a battery implanted on or adjacentto the electrode, or the power source may be implanted at a remote siteon the head or body away from the site of the electrical stimulation, asis currently done for power supplies for cardiac pacemakers and deepbrain stimulators. The electrode is then connected to the remotelyplaced battery using wires. However, it should be understood that futuretechnologies may be employed to provide alternative power sources. Forexample, it may become possible to obtain the energy needed to power theelectrode directly from living tissues surrounding the electrode, suchas nervous tissues, bony tissues, or fibrous tissues.

When the electrode is activated, the output of the electrode is directlyapplied to the SPG, SPN and/or VN, and acts to suppress the painexperienced by the patient by “blocking” the SPG, SPN or VN,respectively. As used herein, the terms “block”, “blocking,” and“blockade” refer to the disruption, modulation and inhibition of nerveimpulse transmissions. As unregulated and increased nerve transmissionis essential for the body to propagate and recognize pain, by blockingnerve impulse transmissions through the SPG, SPN, and/or VN, theinventive method can diminish the pain experienced by the patient.

As the exact parameters of the signal stimulation which may be mosteffective for a particular patient may vary, in the preferred embodimentthe electrode is controllable such that the electrode signal can beremotely adjusted to desired settings, so that no retrieval of theelectrode from the patient is necessary to adjust the patient's therapy.Remote control of the electrode output can be effected, for example,using either conventional telemetry with an implanted electrical signalgenerator and battery or using an implanted radiofrequency receivercoupled to an external transmitter. It should be understood that asrelated technologies advance, other modalities for remote control of theelectrode may be employed to adjust and modulate the electrode'sparameters.

The electrode may be mono-polar, bipolar, or multi-polar. However, it ispreferred that a multi-polar electrode be used as lower current levelsare needed to stimulate the tissue. The electrode and, if desired, anycasing housing the electrode, are preferably made of inert materials(such as, for example, silicon, metal, or plastic), to reduce the riskof triggering an immune response by the patient to the implantedmaterials.

When stimulation is to be applied, the electrode is controlled toproduce an electronic current wave. Preferably, the current wave willcomprise relatively high frequency pulses with a low frequency amplitudemodulation. While the exact parameters for the electrical stimulationare not yet known and are likely to vary by patient, based upon dataknown for stimulations performed on the brain, spinal cord, and cranialnerves, optimal settings for stimulation of the SPG, SPN, and/or VN mayfall in the range of an intensity of about 0.1-20 volts, a frequency ofabout 1-1000 Hertz, and a pulse width of about 25-1000 microseconds.Additionally, it may be effective to produce high frequency bursts ofcurrent on top of an underlying low frequency continuous stimulus.

A variety of methods may be used to surgically implant the electrode onor adjacent to the SPG, the VN, or the SPN. Because the SPG, VN, and SPNare in very close proximity to one another within a very small area, thesame technique is generally applied to achieve placement of theelectrode on or adjacent to any of the three structures. Accordingly,for purposes of the following discussion, it shall be assumed that theinventive method of surgical implantation is being used to implant theelectrode on or adjacent to the SPG, except where specific details areprovided where applicable for use of the implantation method to implantthe electrode on or adjacent to the SPN or VN. It should also beunderstood that, because the region in which the SPG, VN, and SPN alljoin together is very small, stimulation of the SPG, VN, or SPN evenwhen the electrode is placed optimally may also stimulate one or both ofthe other structure.

The inventive method of surgical implantation preferably involveslocalization of the SPG, positioning the electrode on or adjacent to theSPG, and attaching the electrode to a power source. However, with regardto attaching the electrode to a power source, it should be understoodthat electrodes may be developed which make the implantation and/orattachment of a separate power source unnecessary. For example, anelectrode may be used which contains its own power source, which iscapable of obtaining sufficient power for operation from surroundingtissues in the patient's body, or which can be powered by bringing apower source external to the patient's body into contact with thepatient's skin, such as at the cheek. In that case, the surgicalprocedure may be completed upon implantation of the electrode on oradjacent to the SPG.

Electrodes suitable for use with the inventive method include, but arenot limited to, a multipolar electrode which is approximately 1.3millimeters in diameter and has 4 exposed cylindrical electricalcontacts approximately 1.5 millimeters in length, with a 0.5 millimeterinterstice between contacts. The multipolar electrode will thus yield atotal of 7.5 millimeters of distal lead length that can be employed toselectively stimulate the SPG (or SPN or VN, if applicable).

An electrode introducer needle is used to implant the electrode on orproximate to the SPG. A preferred electrode introducer needle is a22-gauge needle which is 10 cm long and has a stylet. As an example,such an electrode introducer needle is available from Radionics in theSluyter-Mehta kit as SMK 100 mm 2 mm active tip cannula. However, itshould be understood that other electrode introducer needles may be usedas appropriate to the needs and skill level of the practitionerperforming the surgical procedure. For example, a needle with a smallerdiameter, such as a 12-gauge, 14-gauge, 16-gauge, 18-gauge, or 20-gaugeneedle, may be used depending upon the diameter of the electrode to beimplanted; however, the smaller diameter needles may be more difficultto manipulate and thus may require a greater skill level on the part ofthe practitioner.

At least one scanning apparatus, such as a CT scan or fluoroscope ispreferably used to monitor the surgical procedure during thelocalization of the SPG. For clarity, the preferred method will bedescribed here using a fluoroscope, but it should be understood that themethod can be readily adapted for use with a CT scan. The patient isplaced supine on a fluoroscopy table, with the patient's nose pointingvertically. The head is then fixed in place on the fluoroscopy tableusing, for example, a strip of adhesive tape. The fluoroscope (which maybe, for example, a fluoroscopy c-arm unit) is then adjusted to astraight lateral position. Referring to FIG. 1, in the lateral position,the sphenopalatine fossa 126 appears as a wedge-shaped structuresituated at the tip of the petrous bone 144 just inferior to theanterior aspect of the sphenoid sinus 146. The x-ray beam of thefluoroscope should then be directed towards the sphenopalatine fossa126. The SPG 102 is situated deep in the sphenopalatine fossa 126. Amarker and a metal ruler are then used to draw a line on the patient'sskin over the sphenopalatine fossa 126. The entry point for theinsertion of the electrode is defined by the intersection of that linewith the inferior edge of the zygomatic arch 116.

This entry point for the insertion of the electrode is located in thecoronoid notch 104 between the condylar 108 and coronoid processes 110of the ramus of the mandible 112. Accordingly, as an alternative oradditional method for identifying the entry point, the coronoid notch104 may be localized by having the patient open the mouth wide andpalpating the mandibular condyle (which is just anterior and inferior tothe external auditory canal 114) as the mandibular condyle movesanteriorly away from the external auditory metus. When the patient thencloses the mouth, the mandibular condyle will move back into place,leaving the entry point into the pterygopalatine fossa 126 (see alsoFIG. 2) through the coronoid notch 104 clear.

Once the entry point is localized, the skin overlying the entry point isshaved and prepared with antiseptic solution. A 25-gauge needle is usedto inject a subcutaneous local anesthetic (such as, for example, 2 cc of2% lidocaine) into the skin and subcutaneous tissues overlying the entrypoint. In addition to the local anesthetic, the patient may be givenintravenous sedation and prophylactic antibiotics prior to commencementof the implantation procedure if desired.

The electrode introducer needle is inserted at the entry point andadvanced between the coronoid process 110 and the condylar process 108of the ramus of the mandible 112 towards the sphenopalatine fossa 126.The electrode introducer needle is slowly advanced in the medial fashionperpendicular to the skin in the anterior-posterior (transverse) planealong the direction of the x-ray beam of the fluoroscope until it entersthe sphenopalatine fossa 126.

The electrode introducer needle is then advanced further into thepterygopalatine fossa 126, at which time it will make contact with themaxillary nerve 140. The patient, upon contact, may report sharp,shooting pain and/or parasthesias in the maxilla 146. Preferably, atthis point an anesthetic solution (such as, for example, 0.5 to 1 cc of1 to 2% zylocaine or lidocaine) is administered through the electrodeintroducer needle to anesthetize the maxillary nerve 140 so that theelectrode introducer needle can be advanced further into thesphenopalatine fossa 126 without producing significant pain in thepatient.

The fluoroscope is then adjusted to an anterior-posterior position. Theelectrode introducer needle is advanced further in a medial fashionuntil it is just adjacent to the lateral aspect of the nasal cavity. Theelectrode introducer needle should be advanced 1 to 2 mm at a time untilit just slips into the sphenopalatine foraminal opening within thelateral aspect of the nasal cavity. The electrode introducer needle mustremain lateral to the nasal mucosa. The fluoroscopic images produced bythe fluoroscope should be consulted frequently during this procedure tomonitor the course of the electrode introducer needle.

If, during this procedure, the electrode introducer needle contactsbone, the needle should be repositioned until it moves into thesphenopalatine foraminal opening. Usually, this will be accomplished bymoving the electrode introducer needle into a more superior and anteriorposition.

If, during the procedure, the needle is about to pierce the nasal mucosabetween the superior 136 and middle 138 nasal turbinates, the needlewill bulge medially into the nasopharynx, indicating that furtheradvancing the needle may pierce the nasal mucosa. If desired, a nasalendoscope can be used in combination with the fluoroscope to show theexact placement of the lateral nasal mucosal wall in order to ensurethat the nasal mucosa is not pierced by the electrode introducer needle,in order to preserve the sterility of the surgical procedure.

Once the electrode introducer needle has been positioned in thesphenopalatine foraminal opening, if it is desired to place theelectrode on or adjacent to the SPN 105, the needle should be furtherdirected to a slightly superior position. If it is desired to place theelectrode on or adjacent to the VN 132, the needle should be directedslightly posteriorly to the opening of the Vidian canal 130. Althoughthe resolution of the fluoroscopy may be limited, it may be used toverify the positioning of the needle on or proximate to the SPG 102, SPN105 or VN 132. In this regard, a CT-scan with very thin slices may offera higher resolution than fluoroscopy and allow more accurate exactpositioning of the needle on or adjacent to the SPG 102, SPN 105 or VN132.

Once the needle is positioned according to whether implantation isdesired on or adjacent the SPG 102, SPN 105 or VN 132, the stylet iswithdrawn from the electrode introducer needle. An electrode used totest the placement of the electrode introducer needle is then placedwithin the central channel of the needle. The electrode is then advancedto the distal tip of the needle to place the electrode on or proximateto the desired structure.

Preferably, the electrode used to test the placement of the electrodeintroducer needle is a radiofrequency stimulating electrode suitable toelectrically stimulate the tissue at the end of the tip of the electrodeand verify its position physiologically within the patient, which may bea different electrode than that ultimately implanted within the patient.A suitable radiofrequency stimulating electrode will be 10 cm with a2-mm non-insulated active tip. The electrode should fit the full lengthof the central channel of the needle with its non-insulated active tipprotruding through the tip of the needle to expose the electricalcontacts. A suitable electrode is produced by Radionics as the 100 mmthermocouple electrode in the SMK kit.

Once the electrode is inserted through the electrode introducer needlewith its electrical contacts exposed, it is then connected to anelectrical stimulus/lesion generator for electrical stimulation. Asuitable electrical stimulus/lesion generator is produced by Radionicsas its RFG 3B model. The frequency of stimulation is set at 50 Hertz andthe voltage is gradually increased until the patient reports tinglingeither in the nose or the soft palate. This tingling should occur at avoltage of less than one volt. If the patient experiences tingling,buzzing, or vibratory sensation just behind the nose, the electrode isin the region of the SPG 102. If the patient reports tingling in thesoft palate, then to position the electrode on or proximate to the SPG102, the electrode must be advanced a few millimeters to reach the SPG102.

If it is desired that the electrode be positioned on or adjacent to theSPN, sensation in the palate is a likely indicator of correctpositioning provided that the position of the electrode is medial to themaxillary nerve 140. The SPN 105 is located superiorly to the SPG 102,and to reach the SPN 105, the electrode should be placed superiorly inthe sphenopalatine fossa 126.

If it is desired that the electrode be positioned on or adjacent to theVN 132, it is unlikely that palate sensation will be experienced withthe electrical stimulation. The VN 132 is located in the posterioraspects of the sphenopalatine fossa 126. Accordingly, the electrodeintroducer needle should be placed in the sphenopalatine fossa 126 asposteriorly as possible so that it can be adjacent to the VN 132 as itemerges from the pterygoid canal.

In any case, if the patient experiences parasthesias outside the cheekand/or the upper lip or within the maxillary nerve distribution, thenthe maxillary nerve is being stimulated. In that case, the electrodeshould be repositioned more medially and inferiorly.

To reposition the electrode, it is removed from the electrode introducerneedle while the needle is held in place. The stylet is replaced withinthe central channel of the electrode introducer needle, and the needleis slightly withdrawn and then re-advanced in the desired directionwhile keeping the same trajectory. Then, with the electrode introducerneedle held firmly in place, the stylet is slowly withdrawn, and theelectrode is replaced within the needle. The electrode is insertedthrough the channel of the needle and pushed all the way into the needleto insure the active tip of the electrode is extending beyond the tip ofthe needle. The correct positioning of the needle and the electrode isthen checked again, as described above, using fluoroscopic imaging andelectrical stimulation.

The process of repositioning of the electrode and retesting should becontinued until the current stimulation yields parasthesia in or behindthe nose at the clinically relevant stimulation settings. At this point,the electrode should be in optimal position.

If the electrode used to test the placement of the electrode introducerneedle is a radiofrequency stimulating electrode different from theelectrode to be implanted, the radiofrequency stimulating electrode isthen carefully removed from the electrode introducer needle while thenneedle is held firmly in place to prevent displacement. The electrode tobe implanted is then inserted through the central channel of the needlewhile the needle is held in place at the hub. As there is connectivetissue and fascia around the SPG, it is believed that the electrode willremain in position. Once the electrode to be implanted is in position,preferably the correct positioning of the needle and the electrode isrechecked, as described above, using fluoroscopic imaging and electricalstimulation.

If the electrode used to test the placement of the electrode introducerneedle is the electrode to be implanted, the electrode should be left inthe final test position.

Once the implanted electrode is in place, the end of the electrode thatis outside the skin is carefully held in place against the skin. Theelectrode introducer needle is then slowly removed, leaving theimplanted electrode in place. At this point, if desired, a few smallsubcutaneous sutures may be placed around the electrode to hold it inthe desired position. Preferably the correct positioning of theelectrode is again checked using fluoroscopic imaging and electricalstimulation.

If the electrode moves upon the withdrawal of the needle, the electrodemust be repositioned. To accomplish this, the electrode should beslightly withdrawn, and the electrode introducer needle should bereinserted over the electrode. The electrode is then completely removedand the stylet is placed back into the needle. This allows the needlewith the stylet inside to be used for repositioning rather than usingthe more delicate electrode. The needle is then repositioned, asidentified by fluoroscopy, the stylet is removed and the radiofrequencystimulating electrode (if used for testing; otherwise, the implantedelectrode) is reintroduced into the needle. Electrical stimulation isagain used to verify the optimal location of the electrode. Theradiofrequency stimulating electrode is then removed and the electrodeto be implanted is placed into the channel of the needle. Anotherattempt is then made to remove the needle completely without moving theelectrode out of position.

Once the needle has been completely removed and the implanted electrodeis in the final position, then the proximal part of the electrode thatis coming out of the skin should be secured to the face by adhesivetape. Additionally, a small incision can be made on the face at the areathe electrode exits the face. Then several subcutaneous sutures shouldbe placed around the electrode to hold it in place. Extreme care shouldbe taken during suturing to insure that the electrode is not damaged,kinked, or strangulated.

The distal end of the electrode is then connected to an extension wireor catheter, which is tunneled to the subclavicular area, or anotherregion which will house the device used as a power source for theimplanted electrode.

A tunneling instrument is used to create a subcutaneous “tunnel”starting at the face where the electrode exits the skin and continuingto the scalp, then the neck, and finally to the clavicular area.Tunneling instruments which may be used to make the tunnel tractinclude, but are not limited to, a Tuohy needle or a Portex tunnelinginstrument. The area to be tunneled should be marked and locallysterilized. Adhesive skin drapes may be used over the entire area ofexposure to keep the region sterile. If desired, a local anestheticsolution may be injected along the tract to be tunneled, and thetunneling instrument may be held in place with forceps so that theelectrode can be passed through the tunneling instrument.

The device or devices used to control or stimulate the electrode may besurgically implanted in the desired region by procedures known in theart, such as have been applied in surgical neuromodulation therapiesused to treat Parkinson's disease.

If desired, the above procedure can then be repeated on the patient'sother side to implant an electrode on or adjacent to the patient'sopposing SPG.

In an alternative embodiment of the inventive method, an electrode maybe utilized which, instead of or in addition to delivering electricstimulation to the SPG, SPN, or VN, delivers a medication solution oranalgesic to the SPG, SPN, or VN. For example, an electrode may be usedthat has a small port at its tip which is connected to a reservoir ormedication pump containing a medication solution or an analgesic such asan anesthetic solution. The medication/analgesic delivery electrode maybe implanted using the same procedure described above for the electricalstimulation electrode. If desired by the patient or physician, thereservoir or medication pump may also be implanted in the patient'sbody, as described above for the electrical stimulus generator. Forexample, the reservoir or medication pump may be implantedsubcutaneously but superficial to the anterior layer of the rectussheath in the paraumbilical region of the abdomen. Preferably theelectrode is controllable such that the amount of medication solution oranalgesic applied, the rate at which medication solution or analgesic isapplied, and the time period over which the medication solution oranalgesic is applied can be adjusted.

It should be understood that the alternative method described above forstimulating the SPG, SPN, or VN, which utilizes delivery of a medicationsolution or analgesic from an electrode, may be used alone or inconjunction with the electrical stimulation method described for thepreferred embodiment of the inventive method. For example, an electrodemay be used which is capable of either producing an electrical stimulusor delivering a medication solution or analgesic. As another example,the electrical stimulation method could be applied to the SPG, SPN,and/or VN of one side of a patient's face, while the method utilizingdelivery of a medication solution or analgesic could be applied to theSPG, SPN, and/or VN of the other side of the patient's face.

Although the foregoing invention has been described in some detail byway of illustration for purposes of clarity of understanding, it will bereadily apparent to those of ordinary skill in the art in light of theteachings of this invention that certain changes and modifications maybe made thereto without departing from the spirit or scope of theappended claims.

1. A method for suppressing or preventing pain in a patient, the methodcomprising the steps of: advancing a first electrode, withoutpenetrating the cranium, on or proximate to at least one of thesphenopalatine ganglia, the sphenopalatine nerves, or the vidian nerveson one side of the patient's face; advancing a second electrode, withoutpenetrating the cranium, on or proximate to at least one of thesphenopalatine ganglia, the sphenopalatine nerves, or the vidian nerveson the other side of the patient's face; applying at least one of amedication solution, an analgesic, or an electrical signal to at leastone of the sphenopalatine ganglia, the sphenopalatine nerves, or thevidian nerves through the first electrode; applying at least one of amedication solution, an analgesic, or an electrical signal to at leastone of the sphenopalatine ganglia, the sphenopalatine nerves, or thevidian nerves through the second electrode; disrupting pain signalgeneration in, or transmission through, the at least one of thesphenopalatine ganglia, sphenopalatine nerves, or vidian nerves on theone side of the patient's face; and disrupting pain signal generationin, or transmission through, the at least one of the sphenopalatineganglia, sphenopalatine nerves, or vidian nerves on the other side ofthe patient's face; wherein each of the first and second electrodes isadvanced without penetrating the nasal cavity or the palate.
 2. Themethod of claim 1 further comprising the step of: applying an electricalsignal through each of the first and second electrodes.
 3. The method ofclaim 1 further comprising the steps of: applying an electrical signalthrough the first electrode; and applying a medication solution oranalgesic through the second electrode.
 4. The method of claim 1 furthercomprising the step of: applying a medication solution or analgesicthrough each of the first and second electrodes.
 5. The method of claim1 further comprising the step of: adjusting at least one of the amountof the medication solution or the analgesic applied, the rate ofapplying the medication solution or the analgesic, and the time periodof applying the medication solution or the analgesic.
 6. The method ofclaim 5, the amount of the medication solution or the analgesic applied,the rate of applying the medication solution or the analgesic, and thetime period of applying the medication solution or the analgesic beingcontrollable by a reservoir or a medication pump.
 7. The method of claim1, wherein at least one of the first and second electrodes is remotelycontrolled using a remote control device which is accessible fromoutside the body of the patient.
 8. The method of claim 1, wherein atleast one of the first and second electrodes is powered by a powersource surgically implanted within the patient.